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1 used a decrease of lumenal pH, eliminated by protonophore.
2 ight-induced passive proton flux enhanced by protonophore.
3 (2)-expressing cells with cells exposed to a protonophore.
4 an activity close to that of a commonly used protonophore.
5 ulation, and response of mitochondrial pH to protonophores.
6 d to enable fatty acids to behave as cycling protonophores.
9 lly, the use of a COUPY-caged version of the protonophore 2,4-dinitrophenol allowed us to confirm by
10 osphonium lipophilic cation and releases the protonophore 2,4-dinitrophenol locally in predetermined
11 and reversible activation by the lipophilic protonophore 2-4 dinitrophenol in a pH-dependent manner.
13 ffect on cellular ATP, but rather due to its protonophore activity that leads to cytoplasm acidificat
16 wever, was stimulated about 4-fold by either protonophore and 2-fold by cyanide or increase of pH 7.5
19 spermidine uptake and Hst 5 killing, whereas protonophores and cold treatment reduced spermidine upta
20 f I(H) induced by DNP, FCCP and other common protonophores and find that it is dependent on AAC and U
21 analysis to determine the binding sites for protonophores and long-chain fatty acids, and find that
22 gy dependent as evidenced by inhibition by a protonophore, and (3) uptake is inhibited by high Zn(II)
23 nsensitive to external pH, pretreatment with protonophores, and treatment with sulfhydryl-modifying r
24 ble expression of mrpA increased the rate of protonophore- and cyanide-sensitive Na+ efflux over that
25 ith the potassium ionophore valinomycin, the protonophore carbonyl cyanide 3-chlorophenylhydrazone, a
28 r than the activation due to the addition of protonophore carbonyl cyanide m-chlorophenylhydrazone (C
29 aining the hybrid motor was inhibited by the protonophore carbonyl cyanide m-chlorophenylhydrazone un
31 r proton pump inhibitor, bafilomycin A1, the protonophore carbonyl cyanide m-chorophenylhydrazone or
36 in sulfate-rich medium upon addition of the protonophore carbonyl cyanide4-(trifluoromethoxy)phenylh
37 s inhibited by cold (50% at 4 degrees C), by protonophores (carbonyl cyanide m-chlorophenylhydrazone,
38 brane proton electrochemical gradient by the protonophore, carbonyl cyanide m-chlorophenylhydrazone (
39 lux was elicited through the addition of the protonophore, carbonyl cyanide m-chlorophenylhydrazone.
40 d in wild-type meningococci treated with the protonophore carbonylcyanide m-chlorophenylhydrazone (CC
41 of the operon was induced by ethanol and the protonophore carbonylcyanide p-chlorophenylhydrazone (CC
42 K+H+ exchangers respectively, as well as the protonophore carbonylcyanide-m-chlorophenylhydrazone (CC
43 tionary growth phase or cells treated with a protonophore causing a decrease in cellular ATP predomin
45 nhibiting mitochondrial Ca(2+) uptake by the protonophore CCCP reduced the frequency of GnRH-induced
47 rees C, were warmed to 24 degrees C, and the protonophore CCCP was added (20 microM) followed 2 min l
48 trictly dependent on Na(+), resistant to the protonophore CCCP, and sensitive to the sodium ionophore
49 bstrates was prevented by treatment with the protonophore CCCP, with no accompanying decrease in cell
53 ion could be inhibited by NOS antagonists or protonophore collapse of the mitochondrial membrane pote
54 hstanding, titration of low-G cells with low protonophore concentrations, monitoring respiration and
55 d whether a controlled-release mitochondrial protonophore (CRMP) that produces mild liver-targeted mi
56 l pH or pretreatment of the yeast cells with protonophores did not significantly affect the rate of 1
57 carbonyl cyanide m-chlorophenylhydrazone, a protonophore, dissipated the membrane potential and abol
58 Mg(2+), or low doses of palmitic acid or the protonophore FCCP exacerbated Ca(2+)-induced sustained d
59 he mitochondrial membrane potential with the protonophore FCCP or blocking the mitochondrial Ca(2+) u
61 tion could be blocked with a low dose of the protonophore FCCP, or the mitochondrial KATP channel ant
62 mediated Na(+) influx and was blocked by the protonophore FCCP, thereby implicating mitochondria as t
67 vesicles, GSH is imported via an ATP-driven, protonophore-insensitive, orthovanadate-sensitive mechan
69 a(2+)-independent activity is seen following protonophore-mediated uncoupling, when uncoupling arises
70 n be released from the ER in the presence of protonophore or proton pump inhibitors which increase th
71 ylanilide scaffold, compounds acting only as protonophores or chitinase inhibitors were identified.
73 contrast to the effects of NO, mitochondrial protonophores produced complete depolarizations of mitoc
75 at acidic buffer pH, and highly sensitive to protonophores; saturable as a function of TPP concentrat
77 al depolarization, because nanomolar CCCP, a protonophore, similarly depolarized mitochondria, elevat
78 of the viable cells remained near basal and protonophore stimulated respiration to the same extent a
79 UCP1 and AAC is lacking, I(H) is induced by protonophores such as 2,4-dinitrophenol (DNP) and cyanid
83 as my example, niclosamide, a small molecule protonophore that, uniquely, can "target" all cell membr
84 Mitochondrial uncouplers are small molecule protonophores that act to dissipate the proton motive fo
85 alled CRMP (controlled-release mitochondrial protonophore), that produces mild hepatic mitochondrial
86 lowered ATP concentration during stress and protonophore treatment-induced clgR-pspA expression, sug
87 CCCP (carbonyl cyanide m-chlorophenyl), a protonophore uncoupler that decreases mitochondrial Ca2+
88 and sucrose accumulation was insensitive to protonophores, was comparable in media differing in pota